Diagnosing Non-HFE Hereditary Hemochromatosis

A 63-year-old Caucasian female presented for evaluation of abnormal bile duct appearance on ERCP after being diagnosed with gallstone pancreatitis, duodenal ulcers and gastritis at another hospital

Helpful or Harmful? A Case Report of Nutritional Supplements Causing Drug-Induced Liver Injury

Herbal supplement-induced liver injury represents a growing concern in the body of drug-induced liver injury (DILI) literature, with recent studies in mainland China, Iceland, and the United States reporting estimated rates of herb/dietary supplement-induced liver injury (HILI) between 1.16-6.38 per 100,000 (Björnsson et al., 2013; Shen et al., 2019; Vega et al., 2017). Notably, a recent 2020 study demonstrated an increasing prevalence of hepatotoxicity secondary to herbal and dietary supplements in the US and worldwide (Zheng et al., 2020). Recognizing the hepatotoxicity of various supplements is crucial, given the increasing usage of dietary and herbal supplements and the lack of regulation of herbal supplements in the United States. HRP-AID is marketed as a twice-daily immune system booster to reduce the intensity and frequency of cold sore outbreaks. The product ingredients include 200 mg ascorbic acid, 20 mcg cholecalciferol, 20 mg a-tocopherol, 10 mg pyridoxine HCl, 50 mcg methylcobalamin, 25 mg zinc citrate, 70 mcg selenium, 250 mg L-lysine, 50 mg Astralagus extract (Astragalus membranaceus), 50 mg Echinacea (Echinacea purpurea), 50 mg garlic powder (Allium salivum), 50 mg natural caffeine (coffee arabica), 50 mg olive leaf extract Oleuropin 20% (Olea Europaea), 50 mg oregano powder (Thymus captatus), 50 mg of elderberry extract (Sambucus nigra) and 50 mg Red Panax ginseng extract (Panax ginseng). A literature review demonstrates that this is the first reported case of DILI secondary to HRP-AID supplementation

Role of Probiotics in Non-alcoholic Fatty Liver Disease: Does Gut Microbiota Matter?

Non-alcoholic fatty liver disease (NAFLD) is the hepatic consequence of metabolic syndrome, which often also includes obesity, diabetes, and dyslipidemia. The connection between gut microbiota (GM) and NAFLD has attracted significant attention in recent years. Data has shown that GM affects hepatic lipid metabolism and influences the balance between pro/anti-inflammatory effectors in the liver. Although studies reveal the association between GM dysbiosis and NAFLD, decoding the mechanisms of gut dysbiosis resulting in NAFLD remains challenging. The potential pathophysiology that links GM dysbiosis to NAFLD can be summarized as: (1) disrupting the balance between energy harvest and expenditure, (2) promoting hepatic inflammation (impairing intestinal integrity, facilitating endotoxemia, and initiating inflammatory cascades with cytokines releasing), and (3) altered biochemistry metabolism and GM-related metabolites (i.e., bile acid, short-chain fatty acids, aromatic amino acid derivatives, branched-chain amino acids, choline, ethanol). Due to the hypothesis that probiotics/synbiotics could normalize GM and reverse dysbiosis, there have been efforts to investigate the therapeutic effect of probiotics/synbiotics in patients with NAFLD. Recent randomized clinical trials suggest that probiotics/synbiotics could improve transaminases, hepatic steatosis, and reduce hepatic inflammation. Despite these promising results, future studies are necessary to understand the full role GM plays in NAFLD development and progression. Additionally, further data is needed to unravel probiotics/synbiotics efficacy, safety, and sustainability as a novel pharmacologic approaches to NAFLD

Primary Pancreatic Lymphoma Presenting as Acute Pancreatitis

Primary pancreatic lymphoma (PPL) is a rare extranodal manifestation of any histopathologic subtype of non-Hodgkin lymphoma that predominantly involves the pancreas. Fewer than 2% of extranodal malignant lymphomas and 0.5% of all pancreatic masses constitute PPL.1 Common clinical manifestations include abdominal pain, jaundice, acute pancreatitis, small bowel obstruction, and diarrhea. The clinical and radiologic findings are not pathognomonic, and the diagnosis is established only after histopathologic and cytopathologic examination with confirmatory molecular testing. Although rare, this particular neoplasm is amenable to treatment even in very advanced stages